Studies on Intrarenal Prostaglandins

Iihoshi, Motohiro; Tsuruta, Kazuma; Soejima, Hidehisa; Ikegami, Keiichi

doi:10.1159/000280293

Cited by 2 publications

(1 citation statement)

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“…It is well known that renal prostaglandins (PGs) have vasodilatory, natriuretic, and diuretic effects [1,2], and synthesis and release of them augment in various renal pathological conditions [2][3][4], In experimental renovas cular hypertension produced by constriction of the unila teral renal artery, some participations of renal PGs in the development and maintenance of hypertension have also been suggested [5][6][7][8][9][10]. In experimental renovascular hy pertension, the initial rise of blood pressure is mainly caused by vasoconstriction due to increased angiotensin II, but the mechanism of the maintenance of hyperten sion has not been obvious [11,12].…”

Section: Introductionmentioning

confidence: 99%

Role of Renal Prostaglandin E<sub>2</sub> in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

Yoshida¹,

Soejima²,

Ueda³

et al. 1986

Nephron

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To investigate the role of renal prostaglandin E₂ (PGE₂) in renovascular hypertension, urinary PGE₂ was measured in rabbits with hypertension produced by left renal artery constriction. In the acute phase of renovascular hypetension (1 week after the constriction), urinary excretions of PGE₂ and sodium were significantly increased without correlations with changes in the systemic blood pressure (ΔBP). In this phase, ΔBP was directly proportional to plasma renin activity and plasma aldosterone concentration (p < 0.001). In the intermediate phase (5 weeks), ΔBP lost significant correlations with plasma renin activity and plasma aldosterone concentration and had a inverse correlation with urinary sodium excretion (p < 0.01). In the maintenance phase (10 weeks), ΔBP showed inverse correlations (p < 0.01) with both PGE₂ and sodium excretions, although their excretions decreased to normal levels. In the clipped kidney, only urinary PGE₂ excretion in the acute phase was significantly elevated (p < 0.02), and both sodium and PGE₂ excretions were significantly decreased (p < 0.01) in the maintenance phase. In the nonclipped kidney, urinary PGE₂ and sodium excretions were elevated in the acute and intermediate phases, but decreased to the control levels in the maintenance phase. In this phase, ΔBP showed inverse correlation (p < 0.01) with both PGE₂ and sodium excretions from the nonclipped kidney. The infusion of saralasin, an angiotensin II analogue, dose dependently reduced the blood pressure in the acute phase, but showed no effect in the intermediate and maintenance phases. The present data suggest that the renin-angiotensin system chiefly contributes to the development of hypertension in the acute phase. However, elevated renal PGE₂ may also partially act as a defensive factor by promoting urinary sodium excretion. In the maintenance phase, the reduced level of urinary sodium excretion in the nonclipped kidney, which has significant correlation with the reduced level of PGE₂, may play an important role to maintain hypertension instead of the renin-angiotensin system.